[Frontiers in Bioscience S3, 276-285, January 1, 2011]

WNT signaling and the regulation of ovarian steroidogenesis

Evelyne Lapointe, Derek Boerboom

Centre de Recherche en Reproduction Animale, Faculte de Medecine Veterinaire, Universite de Montreal, Saint-Hyacinthe, Quebec, Canada, J2S 7C6

TABLE OF CONTENTS

1. Abstract
2. Introduction
2. Introduction
2.1. Steroidogenesis in the growing follicle
2.2. Steroidogenesis in the corpus luteum
2.3. WNT/CTNNB1 signaling
3. WNT signaling in the ovary
3.1. Ovarian WNT signals that regulate steroidogenesis
4. Ovarian WNT signaling mechanisms; interactions with gonadotropin signaling?
4.1. PKA/CREB
4.2. PI3/AKT
4.3. NR5A1 and NR5A2
5. Concluding remarks
6. Acknowledgments
7. References

1. ABSTRACT

One of the major functions of the ovary is the biosynthesis of steroid hormones, which are essential for the development of secondary sexual characteristics at puberty, for subsequent ovarian function, and for the establishment and maintenance of pregnancy. Increases in our understanding of the molecular mechanisms governing the control of ovarian steroidogenesis have greatly improved our understanding of the female reproductive cycle, as well as the pathogenesis of reproductive disorders such as polycystic ovarian syndrome and premature ovarian failure. The pituitary gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH) are the main endocrine regulators of ovarian steroidogenesis, and act by directly or indirectly modulating the activity of a multitude of intracellular signaling pathways. The WNT/CTNNB1 pathway, which is now believed to be a significant contributor to the regulation of ovarian steroidogenesis, could be one of the pathways modulated by gonadotropin signaling. This review will focus on the emerging role of WNT/CTNNB1 signaling in the regulation of steroidogenesis, with emphasis on potential mechanisms of interaction with FSH/LH signaling in ovarian granulosa and luteal cells.